Delayed hemodynamic responses in schizophrenia
Delayed hemodynamic responses in schizophrenia
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DOI：
10.1016/j.neuroimage.2005.03.001
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发表时间：
2005-07-01
期刊：
影响因子：
5.7
通讯作者：
Mathalon, DH
中科院分区：
文献类型：
--
作者：
Ford, JM;Johnson, MB;Mathalon, DH
虽然有许多关于精神分裂症血流动力学反应幅度降低的报道，但没有关于延迟血流动力学反应的报道，尽管事件相关脑电位（ERP）证据表明神经反应减慢。最近，Henson等人（2002）[Henson，R.，普莱斯，C.，Rugg，M.，特纳河，巴西-地弗里斯顿，K.，2002.检测事件相关BOLD反应的潜伏期差异：应用于单词与非单词以及初始与重复的面部呈现。NeuroImage，15：83-97]提出了一种用于测试血液动力学反应中的小潜伏期效应（< 2 s）的新方法。fMRI数据是在视觉古怪任务中收集的，具有不频繁（12%）目标（K）和频繁（88%）标准（X），每1- 3s伪随机呈现，目标之间间隔7-24 s。SPM 99产生了血流动力学反应及其时间导数（TD）的参数估计值。反映对目标刺激的血流动力学反应幅度的Beta图像被最小阈值化（P < 0.05，未校正），并使用TD和血流动力学反应Beta值估计存活体素的潜伏期。DSM-IV精神分裂症患者（n = 12）和性别和年龄匹配的健康对照组（it = 12）从社区招募。虽然组间激活高度差异很小，但精神分裂症患者基底节、丘脑和前扣带回的血流动力学反应明显延迟。在对照组中，对磁体外记录的目标的反应时间反映的心理减慢与基底神经节、前扣带回、丘脑以及左侧小脑的血流动力学减慢有关。血流动力学反应的延迟对于理解精神分裂症的病理生理学具有深远的影响，从神经反应减慢到底物递送减慢，并且取决于延迟的程度，可能会引起关于患者和对照的血流动力学反应建模的方法学问题。(c)2005年爱思唯尔公司All rights reserved.
While there are many reports of reduced amplitude of hemodynamic responses in schizophrenia, there are no reports of delayed hemodynamic responses, in spite of event-related brain potential (ERP) evidence of slowed neural responses. Recently, Henson et al. (2002) [Henson, R., Price, C., Rugg, M., Turner, R., Friston, K., 2002. Detecting latency differences in event-related BOLD responses: application to words versus nonwords and initial versus repeated face presentations. NeuroImage, 15:83-97] proposed a new method for testing small latency effects (< 2 s) in hemodynamic responses. fMRI data were collected during a visual oddball task with infrequent (12%) targets (K) and frequent (88%) standards (X), presented every 1-3 s pseudorandomly, with 7-24 s between targets. SPM99 yielded parameter estimates for the hemodynamic response and its temporal derivative (TD). Beta images reflecting hemodynamic response magnitude to target stimuli were minimally thresholded (P < 0.05, uncorrected), and latencies were estimated for surviving voxels using TD and hemodynamic response beta values. DSM-IV schizophrenia patients (n = 12) and sex- and age-matched healthy control subjects (it = 12) were recruited from the community. Although groups differed only minimally in activation height, hemodynamic responses were significantly delayed in basal ganglia, thalamus, and anterior cingulate in patients with schizophrenia. Psychomotor slowing reflected in reaction times to targets recorded outside the magnet was related to hemodynamic slowing in basal ganglia, anterior cingulate, thalamus, as well as left cerebellum in controls. Delays in the hemodynamic response have far-reaching implications for understanding the pathophysiology of schizophrenia from slowed neural responses to slowed substrate delivery, and depending of the degree of delay, may raise methodological issues regarding modeling hemodynamic responses in patients and controls. (c) 2005 Elsevier Inc. All rights reserved.